Diabetic Retinopathy - PowerPoint PPT Presentation

Diabetic Retinopathy. Waseem Al-Zamil, MD. the two main types of diabetes : Insulin-dependent diabetes (IDD) : - known as type 1 . - develops most frequently between 10 and 20 years of age . Non-insulin-dependent diabetes (NIDD) : - also known as type 2.

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Diabetic Retinopathy

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the two main types of diabetes : • Insulin-dependent diabetes (IDD): - known as type 1 . - develops most frequently between 10 and 20 years of age . • Non-insulin-dependent diabetes (NIDD): - also known as type 2. - develops most frequently between the ages of 50 and 70 years.

Prevalence • Diabetic retinopathy is a leading cause of new cases of blindness in people aged 20 to 74 years . • It has a considerable impact on both the patient and the society because it typically affects individuals in their most productive years .

Prevalence • Blindness is 25 more common in diabetics than non diabetics. • Prevalence of PDR is much more in type I than type II. • Diabetic retinopathy more sever in type I than type II.

RISK FACTORS • The duration of diabetes : • is the most important factor. • In patients diagnosed as having diabetes before the age of 30 years, the incidence of DR : - after 10 years is 50% - after 30 years is 90%

RISK FACTORS • It is extremely rare for DR to develop within 5 years of the onset of diabetes. • about 5% of Type II have NPDR at presentation perhaps due to the lag between onset and diagnosis.

RISK FACTORS 2 . Glycemic control : • Good metabolic control of diabetes will not prevent DR, although it may delay its development by a few years. • increased severity of diabetic retinopathy is associated with poorer glucose control. • insulin treatment is associated with a decreased risk of either the development or progression of diabetic retinopathy in patients with type 1 diabetes.

RISK FACTORS • With strict control of DM: - risk of developing retinopathy was reduced by 75% . - 50% reduction in the rate of progression of retinopathy in existing retinopathy - early worsening of retinopathy is unlikely to threaten vision . Diabetes Control and Complications Trial Research Group N Engl J Med 1993; 329:977-986.

Ocular Risk Factors • PVD : • due to degenerative changes in the vitreous. • significantly more common in diabetic subjects. • complete PVD may prevent the development of PDR because the hyaloid is needed as a scaffold for retinal neovascularization. • attached posterior hyaloid has also been associated with an increased risk for DME

Ocular Risk Factors • High myopia : • choroidal degeneration and extensive old chorioretinopathy protect against DR. • believed to act in the same manner as pan retinal photocoagulation by reducing the metabolic needs of the retina

Ocular Risk Factors • Removal of cataract : • DR may progress after cataract surgery. • Patient who have CSME, SNPDR or PDR should undergo photocoagulation if the media is sufficiently clear. • If the cataract preclude retina evaluation and treatment, prompt postoperative retinal evaluation and treatment should considered.

PATHOGENESIS • Microvascular leakage : - due to reduction in the number of pericytes . - The pericytes are wrapped around the capillaries and are thought to be responsible for the structural integrity of the vessel wall. - Development of retinal edema requires accumulation of fluid which occurs if : Absorption : Leakage : - Uptake from adjusent capillaries - Healthy RPE cells - Microanurerysms. - Incompetent capillaries

CLINICAL FEATURES • Microaneurysms : - located in the inner nuclear layer . - the first clinically detectable lesions . - small round dots .(20-200 μ) - mostly located near and temporal to the macula. - When coated with blood they may be indistinguishable from dot haemorrhages.

CLINICAL FEATURES • Haemorrhages : The clinical appearance depending on location - 'dot' and 'blot' : * originating from the venous end of the capillaries. *located in the compact middle layers of the retina . - Flame-shaped : * originate from the more superficial precapillary arterioles, follow the course of the retinal nerve fibre layer. (liner disribution)

CLINICAL FEATURES • Hard exudates : - located between the inner plexiform and inner nuclear layers of the retina. (OPL) - They are often distributed in a (circinate pattern) . - The centres of rings of hard exudates usually contain microaneurysms . - Made up of accumulated lipoproteins .

CLINICAL FEATURES • Retinal oedema : • located between the outer plexiform and inner nuclear layers. • Later it may involve the inner plexiform and nerve fibre layers, until eventually the entire thickness of the retina may become oedematous. • with further accumulation of fluid, the fovea assumes a cystoid appearance .

CLINICAL FEATURES • Vascular changes : • venous changes :in the form of 'beading', 'looping' and 'sausage-like' segmentation. • It represent endothelial cell proliferation. • arterioles may also be narrowed and even obliterated, resembling a BRAO . - The most powerful predictors for development of PDR.

CLINICAL FEATURES • Cotton-wool spots : (Soft exudates ) - Nerve fiber layer infarction. - caused by capillary occlusion in the retinal nerve fibre layer. • The interruption of axoplasmic flow caused by the ischaemia, and subsequent build-up of transported material within the nerve axons, is responsible for the white and opaque appearance of these lesions. • Disappear within weeks to months.

CLINICAL FEATURES • New Vessels: • Unlike IRMA, they arise on the retinal surface and may extend or be pulled into the vitreous cavity. • NVD : NV appears on or within one DD of disc margin . • NVE : any other location .

CLINICAL FEATURES • Fibrous Glial proliferation : • Accompained growth of new vessels. • It is proliferation between the posterior vitreous gel and the ILM. • Derived from retinal glial cells and fibrocytes.

MANAGEMENT OF DIABETIC RETINOPATHY • Laser surgery : The treatment of depends on the severity of retinopathy and the presence or absence of CSME, which may be present at any stage .

Macular oedema • defined as the presence of any retinal thickening or hard exudates within one disc diameter (i.e. 1500 µm) of the centre of the fovea. • clinically insignificant macular oedema do not require treatment, only should be followed up at 6 monthly intervals.

Clinically significant macular oedema (CSMO) • defined as the presence of one or more of the following features: • Retinal oedema within 500 µm of the centre of the fovea . • Hard exudates within 500 µm of the fovea, if associated with adjacent retinal thickening (which may be outside the 500 µm limit) . • Retinal oedema that is one disc area (1500 µm) or larger, any part of which is within one disc diameter of the centre of the fovea.

Focal laser photocoagulation • All eyes with CSMO should be considered for treatment with laser photocoagulation irrespective of the level of visual acuity because treatment reduces the risk of visual loss by 50%.

Direct treatment • involves applying laser burns to microaneurysms and microvascular lesions in the centre of rings of hard exudates located between 500 and 3000 µm (two disc diameters) from the centre of the fovea. • - The spot size is : 50-100 µm . - The duration of : 0.10 second or less. - The power : sufficient power to obtain a gentle whitening or darkening of the microaneurysm. - Wave length : green – yallow Argon

Direct treatment • Treatment of lesions between 300 and 500 µm from the centre of the fovea should be considered if CSMO persists, in spite of previous treatment and, if visual acuity is less than 6/12.